cinnarizine and Ischemia

94 patients with Stage II obliterating arteriopathy of the lower extremities, treated with Flunarizine (10-20 mg per diem), were checked every two months for a 6 month period. Of the 76 patients reaching the final check up, 58 had received no previous treatment and 18 had ischemias secondary to reconstructive vascular surgery. Clinical improvement in terms of increased independent mobility and improved Doppler flowmeter pressure readings were noted in both groups. In view of its beneficial effects on blood vessel function in other areas, Flunarizine is felt to be a valuable drug for the treatment of peripheral arteriopathies, both initially and in cases of ischaemia following vascular surgery.

Topics: Aged; Arterial Occlusive Diseases; Chronic Disease; Cinnarizine; Clinical Trials as Topic; Female; Flunarizine; Humans; Ischemia; Leg; Male; Middle Aged; Piperazines; Regional Blood Flow; Rheology; Time Factors; Ultrasonography; Vasodilator Agents

Topics: Arm; Arteriosclerosis; Blood Viscosity; Cinnarizine; Clinical Trials as Topic; Diabetes Mellitus; Double-Blind Method; Erythrocyte Membrane; Humans; Ischemia; Myocardial Infarction; Osmolar Concentration; Piperazines; Rheology; Vasodilator Agents

The anti-hypoxic effect of cinnarizine was studied using the following experimental methods: hypobaric and anoxic hypoxia in mice, complete ischemia by decapitation in mice and hemic hypoxia in rats. Papaverine, xanthinol nicotinate and naftidrofuryl were used as reference drugs. In hypobaric and anoxic hypoxia the interaction of cinnarizine with the effect of prostacyclin (PGI2) was investigated. Cinnarizine showed an anti-hypoxic effect in all the methods used. It was more effective in hypobaric and anoxic hypoxia, in incomplete ischemia by decapitation, and less effective in hemic hypoxia. Cinnarizine potentiated the effect of PGI2 shifting the anti-hypoxic dose-response curve of PGI2 to the left. Suggestions as to the possible mechanism of anti-hypoxic action of cinnarizine are made.

Topics: Animals; Atmospheric Pressure; Brain; Cinnarizine; Drug Interactions; Epoprostenol; Hypoxia; Ischemia; Male; Mice; Nafronyl; Oxygen; Papaverine; Piperazines; Rats; Rats, Inbred Strains; Xanthinol Niacinate

The anti-hypoxic effect of piracetam was studied using the following experimental methods: hypobaric and anoxic hypoxia in mice, complete ischemia by decapitation in mice, incomplete ischemia by bilateral carotid occlusion in rats and hemic hypoxia in rats. Cinnarizine and vinpocetine were used as reference drugs. In hypobaric hypoxia, anoxic hypoxia, and complete ischemia by decapitation the interaction of piracetam with the effect of prostacyclin (PGI2) was investigated. Piracetam showed anti-hypoxic effect in all the methods used. Its effect was greater than that of cinnarizine and similar to that of vinpocetine. Piracetam potentiated the effect of PGI2 shifting the anti-hypoxic dose-response curve of PGI2 to the left.

Topics: Animals; Atmospheric Pressure; Cinnarizine; Drug Synergism; Epoprostenol; Female; Hypoxia; Ischemia; Mice; Mice, Inbred Strains; Piracetam; Pyrrolidinones; Rats; Rats, Inbred Strains; Vinca Alkaloids

Perfusion of the cerebral cortex during closed chest CPR in dogs, generating systolic pressures of 60 to 70 mmHg, is only 10% of pre-arrest blood flow. In contrast, internal cardiac massage produces normal cortical perfusion rates. Following a 20-min perfusion arrest, during pressure controlled reperfusion, cortical flow rates decay to less than 20% normal after 90 min of reperfusion. This appears to be due to increasing cerebral vascular resistance, and is not due to rising intracranial pressure. The post-arrest cortical hypoperfusion syndrome is prolonged with cortical flow remaining below 20% normal up to 18 hr post arrest. The use of a variety of calcium antagonists, including flunarizine, lidoflazine, verapamil, and Mg2+, immediately post-resuscitation maintains cerebral vascular resistance and cortical perfusion at normal levels. A prospective blind trial of the calcium antagonist lidoflazine following a 15-min cardiac arrest in dogs and resuscitation by internal massage, demonstrates amelioration of neurologic deficit in the early postresuscitation period.

Topics: Adenosine Triphosphate; Animals; Brain; Calcium; Cell Membrane; Cerebral Cortex; Cerebrovascular Circulation; Cinnarizine; Dogs; Fatty Acids, Nonesterified; Flunarizine; Heart Arrest; Heart Massage; Hypoxia, Brain; Ischemia; Lidoflazine; Nervous System Diseases; Resuscitation

In 48 cases with well-documented retinal vasculopathy, the therapeutic effect of cinnarizine and flunarizine over a period of several months to 3 years has been clinically evaluated. Objective measurements comprised determination of visual field and acuity, funduscopy, three-mirror funduscopy, and fluorangiography with determination of capillary leakage and circulation time. The most prominent features were disappearance of cotton wool nodules, improvement of visual function and capillary perfusion, inhibition of capillary leakage, and a positive hemokinetic effect in arteriolar, capillary, and venous beds. Degeneration of post-ganglionic fibers was partly restored. In some patients with glaucoma, the aspect of the optic disc was normalized. It is concluded that selective calcium-entry-blockers clearly improve tissue perfusion in ischemic areas.

Topics: Adult; Arterioles; Autonomic Fibers, Postganglionic; Calcium Channel Blockers; Capillaries; Cinnarizine; Diabetic Retinopathy; Female; Flunarizine; Fluorescein Angiography; Humans; Hypertension; Ischemia; Male; Middle Aged; Optic Disk; Retinal Artery; Retinal Vein; Venules

Topics: Blood Viscosity; Cinnarizine; Double-Blind Method; Flunarizine; Humans; Ischemia; Meniere Disease; Physical Exertion; Piperazines; Vasodilator Agents

The effects of twelve substances on local cerebral blood flow (LCBF) were studied in the normocapnic and hypercapnic conscious rabbit. In normocapnia, an increase in LCBF was observed after naftidrofuryl (NAF), cinnarizine (CI), viquidil (VI) and heptaminol acefyllinate (HA). The LCBF was only slightly increased or unchanged after hydrogenated ergot alkaloids (HEA), cyclandelate (CY), hexobendine (HE), ifenprodil (IF), piridoxilate (PI), vincamine (VC) and xantinol niacate (XN). It was reduced by theophylline (TH). In hypercapnia, a more pronounced increase in LCBF than in normocapnia was seen with CY, HE, NAF, and VI and a decrease or lesser effect with HA, IF, VC and XN. The decrease in LCBF with TH was enhanced by hypercapnia. The effects of CI, HEA and PI were not modified. The therapeutic implication of these modifications of drug effects by hypercapnia, is discussed.

Topics: Animals; Brain; Cerebrovascular Circulation; Cinnarizine; Heptaminol; Hypercapnia; Ischemia; Nafronyl; Quinolines; Rabbits